Obstructive sleep apnea is related to alterations in fecal microbiome and impaired intestinal barrier function.

Obstructive Sleep Apnea (OSA) is related to repeated upper airway collapse, intermittent hypoxia, and intestinal barrier dysfunction. The resulting damage to the intestinal barrier may affect or be affected by the intestinal microbiota. A prospective case-control was used, including 48 subjects from Sleep Medicine Center of Nanfang Hospital. Sleep apnea was diagnosed by overnight polysomnography. Fecal samples and blood samples were collected from subjects to detect fecal microbiome composition (by 16S rDNA gene amplification and sequencing) and intestinal barrier biomarkers-intestinal fatty acid-binding protein (I-FABP) and D-lactic acid (D-LA) (by ELISA and colorimetry, respectively). Plasma D-LA and I-FABP were significantly elevated in patients with OSA. The severity of OSA was related to differences in the structure and composition of the fecal microbiome. Enriched Fusobacterium, Megamonas, Lachnospiraceae_UCG_006, and reduced Anaerostipes was found in patients with severe OSA. Enriched Ruminococcus_2, Lachnoclostridium, Lachnospiraceae_UCG_006, and Alloprevotella was found in patients with high intestinal barrier biomarkers. Lachnoclostridium and Lachnospiraceae_UCG_006 were the common dominant bacteria of OSA and intestinal barrier damage. Fusobacterium and Peptoclostridium was independently associated with apnea-hypopnea index (AHI). The dominant genera of severe OSA were also related to glucose, lipid, neutrophils, monocytes and BMI. Network analysis identified links between the fecal microbiome, intestinal barrier biomarkers, and AHI. The study confirms that changes in the intestinal microbiota are associated with intestinal barrier biomarkers among patients in OSA. These changes may play a pathophysiological role in the systemic inflammation and metabolic comorbidities associated with OSA, leading to multi-organ morbidity of OSA.

The Change of Soluble Programmed Death Ligand 1 (sPD-L1) in Plasma of Small Cell Lung Cancer and Its Clinical Significance.

Background soluble programmed death-ligand 1 (sPD-L1) expression in lung squamous cell carcinoma and lung adenocarcinoma is associated with disease progression, and sPD-L1 expression in small cell lung cancer (SCLC) may have similar manifestations and become a potential marker for treatment. The purpose of this study was to observe the changes of plasma sPD-L1 expression in SCLC patients. Methods. 90 patients diagnosed with SCLC from January 2019 to November 2020 were selected as the test group, including 72 males and 18 women, 58.7 ± 6.6 years; 30 healthy subjects were selected from the physical examination center, including 18 males, 12 females, and 60.3 ± 7.0 years. There were no statistical difference in sex and age factors between the trial and control groups (p > 0.05). Selected SCLC used chemotherapy regimen: cisplatin + etoposide (EP), carboplatin + etoposide (CE), and SCLC group were divided into three subgroups of disease progression group, partial remission group, and disease stability group according to the treatment effect. Comparison of the differences in sPD-L1 expression content between the experimental and control populations. Plasma sPD-L1 levels were dynamically monitored pre- and posttreatment in 90 patients with small-cell lung cancer and were associated with efficacy among subgroups. Meanwhile, the risk factors for patient sPD-L1 expression content were analyzed by logistic regression. Results. Plasma sPD-L1 levels were higher in the SCLC group than in the healthy people group (t = 7.40, p < 0.01). In the disease progression group of the SCLC group, sPD-L1 levels were decreased in the SCLC group, sPD-L1 in some remission group was increased after treatment, and sPD-L1 levels in the disease-stable group (p > 0.05). Multivariate logistic regression analysis showed that factors promoting increased sPD-L1 expression in SCLC patients included increased smoking, brain metastasis, and ProGRP expression (both p values < 0.05). Conclusion. (1) Higher peripheral sPD-L1 expression in SCLC patients than in healthy patients, and the expression levels were closely related to efficacy. (2) Dynamic changes in s PD-L1 were correlated with clinical efficacy. (3) The progression of sPD-L1 and ProGRP in SCLC patients showed the same extent during remission and stabilization, suggesting the effect of s PD-L1 in the evaluation of SCLC tumors and the reflection of the tumor marker ProGRP.

High miR-3648 expression and low APC2 expression are associated with shorter survival and tumor progression in NSCLC.

BACKGROUND: Emerging studies have demonstrated that microRNAs (miRNAs) play crucial roles in the carcinogenesis of many developing human tumors. However, the clinical significance and biological function of microRNA-3648 (miR-3648) in non-small cell lung cancer (NSCLC) have been largely undefined. METHODS: The expression of miR-3648 and the mRNA of adenomatous polyposis coli 2 (APC2) in NSCLC tissues and cell lines were analyzed using quantitative real-time RT-PCR. The prognostic value of miR-3648 and APC2 was examined using the Kaplan-Meier method and Cox regression analyses. Experiments using NSCLC cells were conducted to explore the influences of miR-3648 on tumor cell proliferation, migration and invasion. RESULT: Increased expression of miR-3648 was observed in NSCLC tissues and cell lines compared with the corresponding controls (all P<0.05). miR-3648 expression was associated with the differentiation, lymph node metastasis and TNM stage (all P<0.05) of NSCLC patients, and high expression of miR-3648 was associated with poor overall survival rate. NSCLC cell proliferation, migration and invasion were significantly enhanced by miR-3648 overexpression. The further luciferase reporter assay and expression results showed that the decreased APC2 might also be a prognostic biomarker, and served as a target of miR-3648 in NSCLC. CONCLUSION: The findings from the present study indicate that the overexpression of miR-3648 serves as a useful biomarker for the prediction of prognosis in NSCLC, and promotes tumor cell proliferation, migration and invasion. APC2, as another prognosis-related molecule, may be a target of miR-3648 in NSCLC.

Identification of a prognostic long noncoding RNA signature in lung squamous cell carcinoma: a population-based study with a mean follow-up of 3.5 years.

BACKGROUND: Lung squamous cell carcinoma (LSCC) is a form of cancer that is associated with high rates of relapse, poor responsiveness to therapy, and a relatively poor prognosis. The relationship between long non-coding RNA (lncRNA) expression and LSCC patient prognosis remains to be established. METHODS: In the present study, we discovered that lncRNAs were differentially expressed in LSCC tumor tissues relative to normal control tissues, and we explored the prognostic relevance of these lncRNA expression patterns using data from the Cancer Genome Atlas (TCGA). RESULTS: These multidimensional data were analyzed in order to identify lncRNA signatures that were associated with LSCC patient survival outcomes. Kaplan-Meier survival curves revealed prognostic capabilities for three of these lncRNAs (LINC02555, APCDD1L-DT and OTX2-AS1). A Cox regression analysis revealed this three-lncRNA signature to be significantly associated with patient survival. Further GO and KEGG analyses revealed that the predicted target genes of these three lncRNAs were also potentially involved in cancer-associated pathways. CONCLUSIONS: Together these results thus indicate that this novel three-lncRNA signature can be used to predict LSCC patient prognosis.

Serum WFA+ -M2BP levels for evaluation of early stages of liver fibrosis in patients with chronic hepatitis B virus infection.

BACKGROUND & AIMS: Accurate evaluation of liver fibrosis is crucial for predicting progression of chronic hepatitis B virus (HBV) infection. We assessed the utility of a novel fibrosis glycobiomarker Wisteria floribunda agglutinin-positive Mac-2-binding protein (WFA+ -M2BP) for evaluating liver fibrosis and disease progression in patients with chronic HBV infection. METHODS: We enrolled 774 patients with chronic HBV infection, with or without fibrosis, diagnosed by liver biopsy/FibroScan. Patients who underwent liver biopsy (n = 297) were divided into training (n = 221) and validation (n = 76) groups. Serum WFA+ -M2BP values were measured and compared with FIB-4 index, aspartate aminotransferase (AST)-to-platelet ratio (APRI) and AST-to-alanine aminotransferase ratio (AAR) using receiver-operating characteristic (ROC) analysis. RESULTS: Serum WFA+ -M2BP levels increased significantly with fibrosis progression (P < 0.0001). Area under the ROC curve of WFA+ -M2BP for diagnosing significant fibrosis was higher than that of FIB-4 (P = 0.198), APRI (P = 0.017) and AAR (P < 0.001), with sensitivity and specificity in the training set of 60.5% and 79.8% and validation set of 59.5% and 82.1%, respectively. Serum WFA+ -M2BP levels were significantly correlated with FibroScan values (P < 0.0001) and improved the accuracy of FibroScan in assessing significant fibrosis. Changes in WFA+ -M2BP levels were parallel with those in FibroScan values during nucleot(s)ide analogues therapy in patients with chronic HBV infection. CONCLUSIONS: WFA+ -M2BP is an accurate serum indicator for assessing early stages of liver fibrosis and may monitor regression of fibrosis during the treatment of chronic HBV infection. WFA+ -M2BP provides a simple and reliable alternative or complementary method to liver biopsy and FibroScan.

[The influence of high birth weight on the blood pressure during childhood - a cohort study].

OBJECTIVE: To explore the effects of high birth weight (HBW) on blood pressure (BP) during childhood. METHODS: A total of 1435 couples with high or normal birth weight were selected from a birth cohort who were born between 1993 and 1995 in Wuxi, China and, followed between 2005 and 2007. A questionnaire survey was conducted, with their height, weight and blood pressure measured. RESULTS: The medians of systolic blood pressure (SBP) and diastolic BP (DBP) of HBW group were 100 mm Hg (Q(1)-Q(3): 90 - 110 mm Hg), 64 mm Hg (Q(1)-Q(3): 60 - 70 mm Hg) in the high birth weight group, respectively, while they were 100 mm Hg (Q(1)-Q(3): 90 - 108 mm Hg), 62 mm Hg (Q(1)-Q(3): 60 - 70 mm Hg) in the normal weight group. No statistical significant difference was found between the exposed and unexposed groups. The proportion of elevated BP, including pre-hypertension and hypertension, in exposed group was 13.66%, a bit higher than that (11.57%) of the unexposed group (P = 0.055). The relative risk (RR) of HBW on elevated BP was 1.06 (0.92 - 1.21), after adjusted the following parameters as BMI in childhood, sex, age during the follow-up period, age of mother at delivery, gestational age, type of feeding at infancy, dietary habit as well as the frequencies of exercise during childhood. CONCLUSION: No statistically significant correlation was found between high birth weight and blood pressure of children.